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SUMMARYA series of herpes simplex virus isolates were recovered from a bone marrow transplant patient who received prolonged acyclovir therapy for indolent herpes simplex mouth and throat ulceration. Of 14 isolates received 10 were resistant to acyclovir and partially resistant to phosphonoacetic acid. Biochemical characterization revealed that resistance was due to an alteration in the virus DNA polymerase. DNA sequence analysis of the polymerase gene of a plaque-purified resistant virus isolate revealed a single nucleotide change when compared with the sequence of the gene of a plaque-purified sensitive isolate. This single base change resulted in a predicted amino acid substitution of Gly to Ser at residue number 841, a putative functional region of the polymerase.

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A simple plaque-reduction assay was used to determine the acyclovir sensitivity of herpes simplex virus isolates taken from patients enrolled int he acyclovir clinical trial programme. The resultant data revealed no reduction in acyclovir sensitivity in virus from those patients, with a normal immune status, receiving topical, oral or intravenous acyclovir for the treatment of acute disease episodes. In the treatment or prophylaxis of chronic herpes infections in immunocompromised patients reductions in sensitivity were observed but these were infrequent. Sensitive virus was later recovered from a small number of patients who had yielded resistant virus when they were followed through to the next recurrence.